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Citations Search

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Nat. Commun. 7, 13665. Acquired RAS or EGFR mutations and duration of response to EGFR blockade in colorectal cancer. 2016

Van Emburgh, B.O., Arena, S., Siravegna, G., Lazzari, L., Crisafulli, G., Corti, G., Mussolin, B., Baldi, F., Buscarino, M., Bartolini, A., Valtorta, E., Vidal, J., Bellosillo, B., Germano, G., Pietrantonio, F., Ponzetti, A., Albanell, J., Siena, S., Sartore-Bianchi, A., Di Nicolantonio, F., Montagut, C. and Bardelli, A.

Notes: The authors purified ctDNA from 1ml plasma using the Maxwell® RSC ccfDNA Plasma Kit with the Maxwell® RSC Instrument. Cell line mismatch repair deficiency was confirmed by the MSI Analysis System, Version 1.2. Cell line authentication was performed using the Cell ID™ and GenePrint® 10 Systems. DNA from cultured and treated cells were purified with the Wizard® SV and SV 96 Genomic DNA Purification Systems. Cetuximab-treated cells were measured for viability with the CellTiter-Glo® Luminescent Cell Viability Assay. (4777)

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Cancer Genomics Proteomics 8, 15–8. BRAF p.Val600Glu (V600E) somatic mutation is mainly associated with MSS phenotype in metastatic colorectal cancer. 2011

Qiu, J., Compagnone, M., Laibe, S., Lagarde, A., Goncalves, A., Turrini, O., Xerri, L., Monges, G. and Olschwang, S.

Notes: The authors amplified and sequenced the KRAS and BRAF genes in 803 patients with metastatic colorectal cancer to determine the frequency of mutation. They also examined the level of microsatellite instability (MSI) in BRAF-mutated cancer samples using the MSI Analysis System, Version 1.1. Of the 34 BRAF-mutated tumors, 8 had microsatellite instability. (4108)

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Am. J. Clin. Pathol. 135, 245–52. KRAS gene mutation in colorectal cancer is correlated with increased proliferation and spontaneous apoptosis. 2011

Liu, X., Jakubowski, M. and Hunt, J.L.

Notes: Mutations in the KRAS gene occur in 30–50% of colorectal cancers. The authors amplified and sequenced the KRAS gene in 198 colorectal cancer samples to detect KRAS mutations. They then determined the frequency of microsatellite instability (MSI) in both KRAS-mutated and KRAS wildtype cancers to show that KRAS-mutated samples had a lower frequency of MSI. MSI analysis of paired normal and cancer tissues were performed using the MSI Analysis System. (4107)

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Anticancer Res. 31, 263–70. Expression of LGR5, an intestinal stem cell marker, during each stage of colorectal tumorigenesis. 2011

Takeda, K., Kinoshita, I., Shimizu, Y., Matsuno, Y., Shichinohe, T. and Dosaka-Akita, H.

Notes: The authors examined the localized expression of Lgr5, a putative cancer marker, in sporadic colorectal adenomas and carcinomas by immunohistochemistry. They also determined the level of microsatellite instability (MSI) in paired normal and tumor tissues using the MSI Analysis System, Version 1.1. Their results showed that the majority of LGR5-positive tumors had low levels of MSI. (4109)

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Am. J. Pathol. 177, 2347–56. Development of sporadic microsatellite instability in colorectal tumors involves hypermethylation at methylated-in-tumor loci in adenoma. 2010

de Maat, M.F., Narita, N., Benard, A., Yoshimura, T., Kuo, C., Tollenaar, R.A., de Miranda, N.F., Turner, R.R., van de Velde, C.J., Morreau, H. and Hoon, D.S.

Notes: The authors examined the methylation status of methylated-in-tumor (MINT) loci and the degree of microsatellite instability (MSI) in colorectal cancer to determine if methylation of MINT loci during the progression of adenoma to cancer was linked to MSI. They used on-slide sodium bisulfite modification and methylation-specific PCR to examine the methylation index in paraffin-embedded tissue blocks containing normal, adenoma and cancer tissues. MSI status was determined using the MSI Analysis System. Patients with instability at more than 4 markers were classified as MSI-high, and patients with instability at more than 1 marker were considered microsatellite-stable. (4106)

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Clin. Can. Res. 16, 1391–401. High-resolution array comparative genomic hybridization in sporadic and celiac disease-related small bowel adenocarcinomas. 2010

Diosdado, B., Buffart, T.E., Watkins, R., Carvalho, B., Ylstra, B., Tijssen, M., Bolijn, A.S., Lewis, F., Maude, K., Verbeke, C., Nagtegaal, I.D., Grabsch, H., Mulder, C.J., Quirke, P., Howdle, P. and Meijer, G.A.

Notes: To better examine the molecular mechanisms of small bowel adenocarcinomas, DNA was extracted from paraffin-embedded tissue and tested for microsatellite instability (MSI) using the MSI Analysis System, Version 1.2. The PCR products were run on the Applied Biosystems 3130 Genetic Analyzer and analyzed using GeneScan® software. If two or more of the BAT-25, BAT-26, NR-21, NR-24 or MONO-27 monomorphic markers had altered lengths, the tumors were designated as MSI unstable. (4112)

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Clin. Can. Res. 16, 5402–13. MSH6 and MUTYH deficiency is a frequent event in early-onset colorectal cancer. 2010

Giráldez, M.D., Balaguer, F., Bujanda, L., Cuatrecasas, M., Muñoz, J., Alonso-Espinaco, V., Larzabal, M., Petit, A., Gonzalo, V., Ocaña, T., Moreira, L., Enríquez-Navascués, J.M., Boland, C.R., Goel, A., Castells, A. and Castellví-Bel, S.

Notes: To better understand early onset colorectal cancer (CRC), the researchers examined mismatch repair (MMR) deficiency by analyzing microsatellite instability (MSI) of five mononucleotide markers BAT25, BAT26, NR21, NR24, and MONO27 from tumors using the MSI Analysis System, Version 1.2. Instability at ≥3 markers classified the tumors as high MSI, while those unstable at ≤2 markers were designated as microsatellite stable. These results were compared with immunostaining analysis of MMR proteins. (4113)

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Mol. Cell. Proteomics 9, 988–1005. Subnuclear proteomics in colorectal cancer: Identification of proteins enriched in the nuclear 2010

Albrethsen, J., Knol, J.C., Piersma, S.R., Pham, T.V., de Wit, M., Mongera, S., Carvalho, B., Verheul, H.M., Fijneman, R.J., Meijer, G.A. and Jimenez, C.R.

Notes: In this paper, the authors were interested in the proteomic analysis of subcellular compartments to see if there were any protein markers for colorectal cancer (CRC) when analyzing early stage tumors and colorectal adenoma and carcinoma tissues. CRC tissue was collected and assessed for microsatellite instability and chromosomal copy number changes using the MSI Analysis System, Version 1.1, and MLPA respectively. The tumor proteins then were analyzed using MALDI-TOF/TOF MS. (4116)

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Otolaryngol. Head Neck Surg. 140, 55–60. Microsatellite instability analysis of sinonasal carcinomas. 2009

Martínez, J.G., Pérez-Escuredo, J., López, F., Suárez, C., Alvarez-Marcos, C., Llorente, J.L. and Hermsen, M.A.

Notes: Because intestinal-type sinonasal adenocarcinoma (ITAC) and squamous cell carcinoma of the nasal cavity (SCCNC) are histopathologically similar to microsatellite-unstable colorectal adenocarcinoma or laryngeal squamous cell carcinoma, respectively, the microsatellite instability (MSI) state of the nasal tumors were of interest to researchers. Two nanograms of purified DNA from 41 ITACs and 24 SCCNCs were amplified for shifts in five mononucleotide microsatellite loci using the MSI Analysis System, Version 1.2. The multiplex PCR products were analyzed by capillary electrophoresis and noted as MSI positive if there was a size shift of at least one marker. (4117)

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J. Mol. Diagn. 10, 301–7. Immunohistochemistry versus microsatellite instability testing for screening colorectal cancer patients at risk for hereditary nonpolyposis colorectal cancer syndrome. Part II. The utility of microsatellite instability testing. 2008

Zhang, L.

Notes: In this review, the author discusses the advantages of the Promega MSI Analysis System, including the use of mononucleotide markers that are monomorphic (i.e., almost all individuals are homozygous for the same common allele) to simplify data analysis. In addition, the inclusion of pentanucleotide repeat markers ensures that the normal and tumor tissue are from the same individual. The author shows representative data generated using MSI Analysis System, Version 1.1. (4118)

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J. Mol. Diagn. 8, 305-11. Comparison of microsatellite instability analysis system and the Bethesda Panel for the determination of microsatellite instability in colorectal cancers 2006

Murphy, KM, Zhang, S, Geiger, T, Hafez, MJ, Bacher, J, Berg, KD, Eshleman, JR

Notes: The researchers compared the Bethesda Panel to Promega's MSI Analysis System (Cat.# MD1641) for the analysis of tissues from 34 colorectal cancers in patients with hereditary nonpolyposis colorectal cancer. (4114)

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Cancer Epidemiol Biomarkers Prev. 15, 2270-3. Somatic BRAF-V600E mutations in familial colorectal cancer 2006

Vandrovcova, J, Lagerstedt-Robinsson, K, Pahlman, L, Lindblom, A

Notes: The authors evaluated the role of oncogenic BRAF mutations in non-hereditary nonpolyposis colorectal cancer/non-familial adenomatous polyposis familial colorectal cancer, by a mutation screening of the most common BRAF mutation, the V600E mutation, in 194 colorectal tumors from patients with a positive family history of the disease. Tumor genomic DNA was isolated and an MSI test performed either as described in the references or using an MSI Analysis System kit (Promega Cat.# MD1641). (4115)

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